Left ventricular (LV) function is of interest for both diagnostic and therapeutic applications. During normal cardiac function, the atria and ventricles operate under consistent time-dependent relationships during the systolic (contractile) phase and the diastolic (relaxation) phase of the cardiac cycle. During cardiac dysfunction such as heart failure (HF) or as associated with diverse pathological conditions (e.g., a myocardial infarction, ischemic event, acute decompensation, etc.) or following cardiac-related surgical procedures, these time-dependent mechanical relationships are often altered. In addition, deleterious remodeling of the myocardium (e.g., LV lateral or “free” wall) oftentimes accompanies HF or other pathological conditions of a patient. This alteration and/or remodeling, when combined with the effects of weakened cardiac muscles or modified depolarization patterns, reduces the ability of the LV to generate contractile strength. Given prior art devices and methods, the resulting hemodynamic insufficiency may require clinical intervention.
Ventricular asynchrony following coronary artery bypass graft (CABG) surgery is a problem encountered relatively often, requiring post-operative temporary pacing. Atrio-biventricular pacing has been found to improve post-operative hemodynamics following such procedures. Chronic cardiac resynchronization therapy (CRT) has been clinically demonstrated to improve indices of cardiac function in patients suffering from congestive heart failure and may promote so-called “reverse remodeling.” Cardiac pacing may be applied to one or both ventricles or multiple heart chambers, including one or both atria, to improve cardiac chamber coordination, which in turn is thought to improve cardiac output and pumping efficiency. Clinical follow-up of patients undergoing resynchronization therapy has shown improvements in hemodynamic measures of cardiac function, LV volumes, and wall motion. However, not all patients respond favorably to CRT. For example, a patient with a LV myocardial infarct (MI) may have altered dispersion patterns of depolarization, left bundle branch block (LBBB), an ectopic site, and/or a reentry circuit related to the MI. Each of which can negatively affect LV activity, both intrinsic and evoked (e.g., by single-site LV pacing). Physicians are challenged in selecting patients that will benefit and in selecting the optimal pacing locations and pacing intervals applied to resynchronize the heart chamber contractions.
The foregoing physiologic issues can negatively affect the efficacious delivery of diverse cardiac stimulation therapies. Thus, a need exists in the art to overcome some or all or of these physiologic issues in order to maximize safe, efficacious and continuous therapy delivery to a patient.
Selection of atrial-ventricular (A-V) and inter-ventricular (RV-LV) pacing sites and intervals (herein “pacing parameters”) oftentimes are based on echocardiographic studies performed to determine the settings resulting in the best acute hemodynamic response. Significant hemodynamic changes may not always be acutely observable in an individual patient, however, using non-invasive monitoring methods. Selection of pacing parameters may therefore be based on avoidance of altered or impeded ventricular filling. In the MIRACLE clinical trial conducted to evaluate CRT, as understood by the inventors, the A-V interval was optimized individually in patients by shortening the A-V interval to maximize ventricular filling without truncating the atrial contribution as observed by echocardiography.
Echocardiographic approaches provide only an open-loop method for optimizing cardiac therapy delivery, such as CRT. After evaluating the hemodynamic effect of varying combinations of pacing parameters, a physician must manually select and program the desired parameters and assume that the patient's device optimal interval settings and electrode location(s) remain unchanged until a subsequent re-optimization visit. Automated systems for selecting timing intervals during multi-chamber pacing have been proposed. A four-chamber pacing system that includes impedance sensing for determining the timing of right heart valve closure or right ventricular (RV) contraction and adjusting the timing of delivery of LV pacing pulses is generally disclosed in U.S. Pat. No. 6,223,082 issued to Bakels et al., incorporated herein by reference in its entirety. Programmable coupling intervals selected so as to provide optimal hemodynamic benefit to the patient in an implantable multichamber cardiac stimulation device are generally disclosed in U.S. Pat. No. 6,473,645 issued to Levine, incorporated herein by reference in its entirety.
In the event that an acute heart failure decompensation event or a spontaneous ventricular tachycardia (VT) occurs, or a patient suffers from an acute Ml, cardiac depolarization and repolarization patterns are typically altered. As a result, an electrical therapy that previously produced effective results (e.g., adequate cardiac output, stroke volume and cardiac perfusion) can be rendered ineffective.
Myocardial acceleration during isovolumic contraction derived from tissue Doppler imaging has been investigated as an index of RV activity. Myocardial acceleration was presumed to be constant during the isovolumic contraction. Doppler tissue imaging has also been used to investigate coordination between septal and lateral wall motion for predicting which patients are likely to benefit from CRT. Evidence suggests patient response is dependent on the degree of ventricular synchrony before and after therapy. Doppler tissue imaging studies have shown that the LV mid-lateral to mid-basal segments show the greatest improvement in shortening following CRT. Detection and monitoring of LV activity, therefore, would be useful in optimizing CRT. Myocardial activity is not as preload-dependent or autonomically sensitive as hemodynamic measures of ventricular function. Optimization of CRT based on myocardial activity is expected to be less transient than optimization based on hemodynamic parameters, which could quickly change under autonomic influence or alterations in preload. Myocardial acceleration, however, is not a constant during isovolumic contraction when measured directly by an accelerometer. Therefore, a method is needed for using signals to monitor myocardial acceleration, particularly in the LV for use in assessing cardiac activity and optimizing CRT.
Implantable sensors for monitoring heart wall motion have been described or implemented for use in relation to the RV. A sensor implanted in the heart mass for monitoring heart function by monitoring the momentum or velocity of the heart mass is generally disclosed in U.S. Pat. No. 5,454,838 issued to Vallana et al. A catheter for insertion into the ventricle for monitoring cardiac activity having an acceleration transducer at or proximate the catheter tip is generally disclosed in U.S. Pat. No. 6,077,236 issued to Cunningham. Implantable leads incorporating accelerometer-based cardiac wall motion sensors are generally disclosed in U.S. Pat. No. 5,628,777 issued to Moberg, et al. A device for sensing natural heart acceleration is generally disclosed in U.S. Pat. No. 5,693,075, issued to Plicchi, et al. A system for myocardial tensiometery including a tensiometric element disposed at a location subject to bending due to cardiac contractions is generally disclosed in U.S. Pat. No. 5,261,418 issued to Ferek-Petric et al. All of the above-cited patents are hereby incorporated herein by reference in their entirety.
Detection of peak endocardial wall motion in the apex of the RV for optimizing A-V intervals has been validated clinically. A system and method for using cardiac wall motion sensor signals to provide hemodynamically optimal values for heart rate and AV interval are generally disclosed in U.S. Pat. No. 5,549,650 issued to Bornzin, et al., incorporated herein by reference in its entirety. A cardiac stimulating system designed to automatically optimize both the pacing mode and one or more pacing cycle parameters in a way that results in optimization of a cardiac performance parameter, including for example heart accelerations, is generally disclosed in U.S. Pat. No. 5,540,727, issued to Tockman, et al.
It is apparent from the above discussion that a need remains for providing a device and method for monitoring myocardial activity in the LV and for selecting optimal cardiac pacing intervals that produce the greatest improvement in LV activity during multi-chamber or biventricular pacing delivered to improve heart chamber output and/or intra-chamber synchronization, chronically or acutely. An improved index of LV activity is expected to reflect an improvement in overall cardiac chamber synchrony and function and generally result in a net improvement in cardiac efficiency.